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Results for “Intranuclear Inclusion Bodies”

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At least 73 records · Page 4Linked to original sources
PubMed1995

The diagnosis of Wesselsbron disease in a new-born lamb by immunohistochemical staining of viral antigen.

Wesselsbron disease (WSL) was diagnosed in a 2-d-old lamb on a farm in the north-eastern Free State Province where a few abortions and neonatal deaths occurred in sheep in April 1994. The liver of the lamb was slightly swollen and orange-brown and, microscopically, it revealed single or small groups of necrotic hepatocytes that were randomly scattered throughout the lobules. Other histopathologic hepatic lesions included the presence of acidophilic bodies, intranuclear inclusion bodies in a few hepatocytes, neutrophils in the parenchyma, mild Kupffer-cell and bile-ductular proliferation and infiltration of mixed inflammatory cells in the portal tracts. Immunohistochemical staining of sections of formalin-fixed specimens of the liver with polyclonal antibody against WSL virus revealed positive staining in acidophilic bodies, cytoplasmic fragments of necrotic liver cells, the cytoplasm of degenerated hepatocytes and, rarely, in intranuclear inclusions. Positive staining was also obtained in liver sections from two newborn lambs experimentally infected with WSL virus. The results of this investigation showed that the immunohistochemical staining of sections of formalin-fixed liver can be used to confirm the diagnosis of WSL in new-born lambs.

Animals↗
PubMedDate not supplied

Pathologic study of specific-pathogen-free chicks and hens inoculated with adenovirus isolated from hydropericardium syndrome.

The mortality and pathology caused by serotype 4 adenovirus, isolated from chickens with hydropericardium syndrome (HPS) in Japan, was investigated in specific-pathogen-free (SPF) chickens. One-day-old to 15-mo-old SPF chickens were inoculated intramuscularly, orally, and intranasally with liver homogenates from HPS chickens or isolated serotype 4 adenovirus. There were no clinical signs before death. The mortality rate in all groups of 1-day-old chicks was 100%, irrespective of the inoculum or inoculation route. Four-week-old chickens inoculated with liver homogenate also had a 100% mortality rate. Five-week-old chickens inoculated with cell culture of HPS adenovirus had a 40% mortality rate. The mortality rates of 7-mo-old hens inoculated with liver homogenates intramuscularly and orally were 75% and 25%, respectively. In 15-mo-old hens inoculated with liver homogenates intramuscularly, the mortality rate was 70%. Gross lesions were hydropericardium and swelling and congestion of the liver with occasional petechial hemorrhages. Histologically, the liver had diffuse or multifocal hepatic necrosis and hemorrhage with intranuclear inclusion bodies noted within hepatocytes. In the spleen, macrophages containing erythrocytes and yellow pigment were prominent in the red pulp. In the lung, a moderate diffuse macrophage infiltration was noted throughout the lung parenchyma, and these macrophages contained yellow pigment. In the pancreas of the chicks inoculated at 1 day old, there was multifocal necrosis of glands with intranuclear inclusion bodies. Intranuclear inclusion bodies were seen also in the gizzard, proventriculus, duodenum, cecum, kidney, and lung of the chicks inoculated at 1 day old. Immunohistochemically, the intranuclear inclusion bodies of various organs showed positive reactions against group I avian adenovirus. Adenovirus was recovered from the liver of chickens with HPS. This study indicates that HPS adenovirus is able to reproduce HPS lesions and mortality in SPF chicks and even adult chickens and that it is a highly pathogenic strain.

Adenoviridae↗
PubMed1992

Inclusion bodies containing adenovirus-like particles in the intestine of a psittacine bird affected by inclusion body hepatitis.

This paper reports a case of inclusion body hepatitis with intranuclear inclusion bodies in the liver and the intestine of a Yellow-naped Amazon parrot (Amazona ochrocephala). Structurally, basophilic intranuclear inclusion bodies were found in hepatic cells and enterocytes. Ultrastructurally, icosahedral adenovirus-like particles, 60-75 nm in diameter, were found in the same cells.

Adenoviridae Infections↗
PubMed1987

Pathological changes in HPCD pigs with prednisolone induced recrudescence of pseudorabies virus.

In HPCD pigs inoculated with PRV, latent PRV could be reactivated in-vivo by the administration of large doses of prednisolone 3 months after the primary infection. In two pigs, virus shedding was without clinical signs of disease, whereas depression of circulating lymphocytes was prominent. Reactivation of PRV was also demonstrated by cultivation of the brain cortex on the 7th day and the mandibular lymph node on the 9th day after the prednisolone began treatment. Coincident with the virus isolation, characteristic lesions were observed in 2 pigs in the central nervous tissues and mandibular lymph nodes and these were composed of cell necrosis and eosinophilic intranuclear inclusion bodies. Cells containing the intranuclear inclusion bodies had immature and mature PRV particles. Results of the present study with HPCD pigs indicated that the lesions in the brain and lymph node accompanied by eosinophilic intranuclear inclusion bodies were pathogonomonic lesions induced by reactivation of PRV.

Animals↗
PubMed1987

Studies on the sequential development of acute interstitial pneumonia caused by Aleutian disease virus in mink kits.

We studied different parameters during the development of acute interstitial pneumonia in mink kits caused by neonatal infection with Aleutian disease virus (ADV). When histological lesions, presence of intranuclear inclusion bodies, and intranuclearly localized ADV antigen were correlated with levels of single-stranded virion and duplex replicative forms of ADV DNA in the different tissues, it was concluded that the lung, probably alveolar type II cells, is the major primary target for viral replication and cytopathology. The presence of the duplex dimeric replicative-form DNA, a strong marker of parvovirus replication, was also observed in low amount in the mesenteric lymph node, suggesting replication of ADV in this organ, although no viral cytopathology could be demonstrated. Moreover, a few intranuclear inclusion bodies were demonstrated in kidney and liver from affected kits, but intranuclearly localized ADV antigen could not be demonstrated in liver sections, and neither could duplex dimer replicative-form DNA, suggesting that these organs are nevertheless not a major site of ADV replication. When the data were compared with results previously reported for ADV-infected adult mink and ADV-infected permissive cell cultures, the data suggested that the pattern of ADV replication in alveolar type II cells is similar to that seen in infected cell cultures but that the replication in the other kit organs resembles the restricted pattern seen in adult mink.

Aleutian Mink Disease↗
PubMed1985

Pathologic changes in pigs with prednisolone-induced recrudescence of herpesvirus infection.

In pigs inoculated with Aujeszky's disease virus (ADV), recrudescence of herpesvirus infection was induced by daily administration of 1,000 mg of prednisolone for 5 days at 2 (group A) or 5 (group B) months after the primary infection. At necropsy in group A pigs, ADV was recovered from nasal secretions 3 to 9 days after prednisolone treatment initiation and from the brain cortex 10 days after treatment initiation; ADV was not recovered from group B pigs. In pigs of both groups killed 10 days after treatment initiation, 2 types of characteristic lesions were found. One type was a nonsuppurative encephalitis that consisted of neuronal necrosis, neuronophagia, and formation of eosinophilic intranuclear inclusion bodies. The 2nd type had basophilic intranuclear inclusion bodies in the enlarged endothelial cells of the kidneys, liver, lungs, adrenal glands, and lymph node sinusoids. Cells containing intranuclear inclusion bodies had immature and mature herpesvirus particles. Therefore, the brain lesions containing the eosinophilic inclusion bodies were considered to be due to ADV. Basophilic inclusion bodies in the endothelial cells were due to porcine cytomegalovirus. These observations indicated that prednisolone treatment resulted in recrudescence of ADV and porcine cytomegalovirus infections.

Animals↗
PubMed2002

Wild rats as monitors of environmental lead contamination in the urban area of Milan, Italy.

Twenty-one wild brown rats (Rattus norvegicus) were collected from four areas of Milan (Italy). Main organs were harvested from each rat, fixed in 10% neutral buffer formalin, and embedded in paraffin. Organ sections were stained with hematoxylin and eosin, kidney sections were also stained with the Ziehl-Neelsen method. Graphite furnace atomic absorption spectrophotometry was performed on all kidney samples. The presence of inclusion bodies and karyocytomegaly was scored. Six adult rats out of 21 (28.6%) showed kariocytomegaly and intranuclear inclusion bodies of the renal proximal tubules, characteristic of lead toxicity. The nuclear inclusion bodies were always Ziehl-Neelsen positive. The six rats which showed the characteristic histological alterations ascribed to lead, had lead concentrations statistically higher than the three control rats (4 microg/g wet wt. versus 0.09 microg/g wet wt., P<0.001) and than the captured wild rats. Intranuclear inclusion bodies were found in rats with kidney lead concentrations greater than 0.6 microg/g wet weight. There were significant differences between the four areas of capture. The incidence of intranuclear inclusion bodies and karyocytomegaly in proximal tubular cells was higher in rats with high lead levels detected by spectrophotometry. The present results indicate a renal lead concentration of 0.6 microg/g wet weight as a threshold to detect histologic kidney changes due to lead absorption. Results demonstrate that the examination of adult free-living rats may be considered an appropriate method to obtain a rapid, sensitive, easy, cost effective estimate of lead contamination in urban areas. Animal models allow us to evaluate potential human health risk associated with environmental contamination.

Animals↗